Open AccessAldehyde dehydrogenase 2 overexpression inhibits neuronal apoptosis after spinal cord ischemia/reperfusion injury
Author(s) -
Xing Zhen Liu,
Xin Sun,
Kangping Shen,
Wenjie Jin,
Zhiyi Fu,
Hairong Tao,
Zhixing Xu
Publication year - 2017
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.211198
Subject(s) - aldh2 , medicine , ischemia , reperfusion injury , spinal cord , anesthesia , agonist , spinal cord injury , oxidative stress , pharmacology , endocrinology , aldehyde dehydrogenase , receptor , biology , biochemistry , psychiatry , gene
Aldehyde dehydrogenase 2 (ALDH 2 ) is an important factor in inhibiting oxidative stress and has been shown to protect against renal ischemia/reperfusion injury. Therefore, we hypothesized that ALDH 2 could reduce spinal cord ischemia/reperfusion injury. Spinal cord ischemia/reperfusion injury was induced in rats using the modified Zivin's method of clamping the abdominal aorta. After successful model establishment, the agonist group was administered a daily consumption of 2.5% alcohol. At 7 days post-surgery, the Basso, Beattie, and Bresnahan score significantly increased in the agonist group compared with the spinal cord ischemia/reperfusion injury group. ALDH 2 expression also significantly increased and the number of apoptotic cells significantly decreased in the agonist group than in the spinal cord ischemia/reperfusion injury group. Correlation analysis revealed that ALDH 2 expression negatively correlated with the percentage of TUNEL-positive cells ( r = -0.485, P < 0.01). In summary, increased ALDH 2 expression protected the rat spinal cord against ischemia/reperfusion injury by inhibiting apoptosis.